心脏重构是肥胖症患者发生心力衰竭的重要原因。我们前期发现脂肪功能障碍触发成纤维细胞激活，内皮细胞ETS-1介导心脏纤维化，但ETS-1在脂肪细胞中的功能未见报道，与肥胖相关性心脏重构的关系尚未阐明。我们在预实验中证实脂肪细胞ETS-1通过PDGF-D调控心脏成纤维细胞激活，提示脂肪细胞ETS-1与心脏纤维化有关。本项目通过脂肪特异性敲除ETS-1小鼠建立高脂饮食诱导肥胖引起的脂肪功能障碍模型，检测心功能、心肌纤维化与肥大以及炎症浸润程度。体外用脂肪特异性敲除ETS-1小鼠的脂肪前体细胞分泌物刺激心脏成纤维细胞，检测细胞增殖、凋亡、迁移和胶原纤、差异蛋白及相关通路的表达，旨在获得脂肪细胞ETS-1影响心脏成纤维细胞激活的可靠依据，阐明脂肪细胞ETS-1影响肥胖相关性心脏重构的新机制，为确立防治肥胖相关性心脏重构的新靶标提供科学依据。

Cardiac remodeling is an important cause of heart failure in obese patients. We previously discovered that adipose tissue dysfunction triggers fibroblasts activation and endothelial ETS-1 mediates cardiac fibrosis. However, the function of ETS-1 in adipocytes has not been reported, and its relationship with obesity-related cardiac remodeling has not been elucidated. Our preliminary experiments found that adipocyte ETS-1 regulates cardiac fibroblasts activation through PDGF-D, suggesting that adipocyte ETS-1 regulates cardiac fibrosis. The purpose of this study was to evaluate the correlation between Ets-1 and cardiac hypertrophy in obese patients and normal subjects, establish a model of adipose tissue dysfunction caused by high-fat diet-induced obesity in adipocyte specific ETS-1 knockout mice, measure cardiac function, myocardial fibrosis and hypertrophy, and inflammatory infiltration. Cardiac fibroblasts were stimulated with adipocyte specific knockout of ETS-1 mice in vitro to stimulate cardiac fibroblasts, and cell proliferation, apoptosis, migration, collagen fibers、differential protein and related signaling pathways were measured in order to obtain a reliable basis for the influence of adipocytes on the activation of cardiac fibroblasts, to clarify the new mechanism of adipocytes affecting obesity-related cardiac remodeling, and to provide a scientific basis for establishing new targets for preventing and controlling cardiac remodeling in the future.